Diabetes Why managing blood sugar is so important.

n.

Any of several metabolic disorders marked by excessive discharge of urine and persistent thirst, especially one of the two types of diabetes mellitus.

[Middle English diabete, from Medieval Latin diabētēs, from Latin, from Greek, siphon, diabetes, from diabainein, to cross over, straddle : dia-, dia- + bainein, to go.]

WORD HISTORY   Diabetes is named for one of its distressing symptoms. The disease was known to the Greeks as diabētēs, a word derived from the verb diabainein, made up of the prefix dia–, “across, apart,” and the word bainein, “to walk, stand.” The verb diabeinein meant “to stride, walk, or stand with legs asunder”; hence, its derivative diabētēs meant “one that straddles,” or specifically “a compass, siphon.” The sense “siphon” gave rise to the use of diabētēs as the name for a disease involving the discharge of excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425.

A condition in which excessive amounts of some substances are excreted from the body. The term may refer to either of two unrelated diseases, diabetes mellitus and diabetes insipidus. In common usage, the term diabetes is synonymous with diabetes mellitus.

Diabetes mellitus

This is a disease of abnormal carbohydrate metabolism in which glucose cannot enter the body's cells and be utilized, and therefore remains in the blood in high concentrations. In diabetes mellitus the excess sugar in the blood (hyperglycemia) leads to the excretion of sugar in the urine (glycosuria), a cardinal diagnostic symptom. Glycosuria in turn causes the excretion of large amounts of urine (polyuria), which results in dehydration and intense thirst (polydipsia). Although blood glucose is high, it cannot enter the appetite-regulating cells of the hypothalamus; hunger is therefore great, and the diabetic person tends to eat constantly (polyphagia). But because glucose cannot enter and nourish the cells, body tissues are subjected to the equivalent of starvation; rapid weight loss occurs, part of which is due to the excretion of water in urine. See also Carbohydrate metabolism.

Diabetes mellitus appears in two varieties, each with its own cause: diabetes mellitus type I (formerly known as juvenile onset diabetes), caused by deficiency of the pancreatic hormone insulin (whose chief function is to promote the entry of glucose into cells); and diabetes mellitus type II (formerly known as maturity onset diabetes), in which insulin is available but cannot be properly utilized. See also Insulin; Pancreas.

Three factors that are believed to be important in the causation of this disease are heredity, viral infections, and immunological damage to the pancreas. Heredity does operate in determining one's risk of diabetes, but only as a predisposing factor, not as an absolute determinant. The two types of diabetes mellitus have entirely different patterns of inheritance. Virus infection is strongly implicated as one causative factor in the beta-cell destruction that characterizes type I diabetes, but it is not involved in type II diabetes. Some of the viruses that have been implicated are the agents of mumps and rubella (German measles) and coxsackievirus B. Autoimmune reactions, wherein the body's immune defense system attacks its own pancreatic tissue as though it were a foreign substance, are also suggested as a cause for the beta-cell destruction of type I diabetes. See also Animal virus; Autoimmunity; Human genetics.

Dietary management has been part of diabetic therapy since preinsulin days, when starvation diets were used to prolong the life of type I diabetics. More recently, weight reduction for victims of type II diabetes and complex carbohydrate liberalization for those of both types of diabetes mellitus have been the cornerstone of therapy. Some other dietary measures besides reducing caloric intake are now believed beneficial for type II diabetics. The ingestion of foods high in fiber content, for example, has been shown to reduce hyperglycemia in type II diabetics. For type I diabetics, the traditional diet is high in protein and quite restricted in carbohydrates. Since most type I diabetics are thin, weight reduction is not part of their program.

Diabetes insipidus

Diabetes insipidus is caused by a deficiency of, or resistance to the action of, vasopressin, the antidiuretic hormone produced by the posterior lobe of the pituitary gland. If the pituitary fails to produce vasopressin, the condition is called central diabetes insipidus. If the kidneys do not respond to the vasopressin and fail to concentrate urine, the condition is labeled nephrogenic diabetes insipidus. Symptoms include increased thirst and frequent urination. Permanent damage to the kidneys can result if the condition is not treated.

A low level of vasopressin can be corrected with desmopressin acetate, a synthetic analog of 8-argininevasopressin, which can be administered in the form of a nasal spray. Desmopressin acetate is ineffective in the treatment of nephrogenic diabetes insipidus. See also Neurohypophysis hormone.

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Diabetes usually refers to the condition known in full as diabetes mellitus. ‘Diabetes’ can be translated, from its Greek derivation, as ‘going through’ — describing the characteristic copious production of urine. ‘Mellitus’ comes from the Latin for honey. There is an excess of sugar (glucose) in the blood and this ‘spills over’ into the urine, bringing an excess of water with it. The cause is either a deficiency of production of the hormone insulin by the pancreas, or defective response of body cells to the action of this hormone, which normally enables glucose and other nutrients to be taken up from the circulating blood. The derangement of metabolism leads to extensive complications. The type of diabetes due to lack of insulin production was fatal before the early 1920s, when treatment with an extract from animal pancreatic tissue was shown to be effective.

The illness with ‘the passing of too much urine’ was known in 1500 bc to the Egyptians; Aretaeus wrote of it in the second century ad as ‘diabetes … a melting down of the flesh and limbs into urine’; Paracelsus described it in the sixteenth century; but it was the English physician Thomas Willis who first reported in 1679 that the urine was ‘so wonderfully sweet’.

A much rarer condition, diabetes insipidus (with copious urine which is not ‘sweet’), is caused by deficiency of antidiuretic hormone (ADH) (also known as vasopressin) from the pituitary gland. ADH normally acts in the kidneys to prevent any greater escape of water in the urine than is necessary to maintain constancy of the salt concentration and volume of the body fluids. When ADH is lacking, due to disease or injury in or near the pituitary gland, the daily output of dilute urine can be 25-30 litres, with extreme thirst to match.

— Stuart Judge

See blood sugar; body fluids; insulin; pancreas; pituitary gland.

There are two distinct conditions: diabetes insipidus and diabetes mellitus. The latter condition is more common, and is generally referred to simply as diabetes or sugar diabetes. Haemochromatosis is known as bronze diabetes.

Diabetes insipidus is a metabolic disorder characterized by extreme thirst, excessive consumption of liquids and excessive urination, due to failure of secretion of the antidiuretic hormone.

Diabetes mellitus is a metabolic disorder involving impaired metabolism of glucose due to either failure of secretion of the hormone insulin (insulin-dependent diabetes) or impaired responses of tissues to insulin (non-insulin-dependent diabetes). If untreated, the blood concentration of glucose rises to abnormally high levels (hyperglycaemia) after a meal and glucose is excreted in the urine (glucosuria). Prolonged hyperglycaemia may damage nerves, blood vessels, and kidneys, and lead to development of cataracts, so effective control of blood glucose levels is important.

Type I diabetes mellitus develops in childhood (juvenile-onset diabetes) and is due to failure to secrete insulin, and hence is called insulin-dependent diabetes. Treatment is by injection of insulin (originally purified from beef or pig pancreas, now biosynthetic human insulin), together with restriction of the intake of sugars.

Type II diabetes mellitus generally arises in middle age (maturity-onset diabetes) and is due to resistance of the tissues to insulin action; secretion of insulin by the pancreas may be normal or higher than normal. It is referred to as non-insulin-dependent diabetes and can sometimes be treated by restricting the consumption of sugars and reducing weight, or by the use of oral drugs which stimulate insulin secretion and/or enhance the insulin responsiveness of tissues (sulphonylureas and biguanides). It is also treated by injection of insulin to supplement secretion from the pancreas and overcome the resistance. Impairment of glucose tolerance similar to that seen in diabetes mellitus sometimes occurs in late pregnancy, when it is known as gestational diabetes. Sometimes pregnancy is the stress that precipitates diabetes, but more commonly the condition resolves when the child is born.

Renal diabetes is the excretion of glucose in the urine without undue elevation of the blood glucose concentration. It is due to a reduction of the renal threshold which allows the blood glucose to be excreted. See also glucose tolerance.

Diabetes is the commonly used abbreviation for the medical condition diabetes mellitus, a disorder characterized by an increased blood sugar level. This may be due to the body's inability to produce enough insulin (called Type I diabetes, insulin-dependent diabetes, or juvenileonset diabetes), or an inability to use insulin properly (called Type II diabetes, adult-onset diabetes, insulin-independent diabetes, or non-insulin-dependent diabetes). In addition to high blood glucose levels, diabetes results in a depression of carbohydrate utilization. This causes the formation of ketones in the liver, toxic chemicals which damage the nervous system and may lead to convulsions and a diabetic coma.

Type I diabetes develops primarily in young people under 30 years and accounts for about 10 per cent of diabetics. Signs and symptoms include weakness and fatigue, irritability, nausea, thirst, and frequent passing of urine. Type I diabetics frequently suffer extreme hunger and weight loss. Consequently, they are typically lean or have a normal body weight. If left untreated, they often have abnormally high levels of potentially toxic ketones in their blood. To counter the pancreas's lack of insulin production, Type I diabetics take artificial insulin to maintain blood glucose concentrations within the normal range. Regular physical activity has been shown to help Type I diabetics control their blood glucose levels. It also reduces the risk of cardiovascular diseases.

Type II diabetes results from a resistance to insulin. It usually develops gradually in people over 40. Its development is sometimes linked to obesity. One of the highest incidence of Type II diabetes in the world is among a group of people in a district of Port Moresby, the capital of Papua New Guinea. In the past, fat was usually in short supply, so it is believed that the people evolved a genetic ability to store fat in times of plenty. This may have predisposed them to diabetes when they adopted a Western, high fat diet. In type II diabetes, the production of insulin by the pancreas may be normal or even greater than normal, but the liver and muscle cells become relatively insensitive to the hormone. Primary treatment of Type II diabetics includes diet and exercise to achieve a desirable body weight, and to control blood glucose. Development of Type II diabetes is less likely in those who lead physically active lives, and physical activity is generally recommended as an effective means of managing the disease. The risk of Type II diabetes falls by about 6 per cent for every 500 Calories of energy expended per week (approximately equivalent to jogging or swimming for an hour). Regular aerobic exercise reduces the concentration of insulin in blood serum, and increases the sensitivity of the cells to insulin. This increased sensitivity applies to diabetics as well as non-diabetics: sedentary diabetics require about 0.5-1.0 insulin units per kilogram; exercising diabetics require 0.5-0.6 units. Exercise may also reduce the risk of cardiovascular complications. The protection provided by exercise is greatest among obese and elderly people, and those with a family history of diabetes.

Although exercise may benefit diabetics, it also presents some dangers. Overexertion may cause hypoglycaemia (low blood glucose) and, paradoxically, in Type II (non-insulin-dependent) diabetics, it can result in hyperglycaemia (high blood glucose) because the exercise reduces insulin production. Clearly, vigorous exercise may not be safe unless blood glucose levels are well controlled. Certain types of high impact exercise, such as road running, may also harm diabetics who have a decrease in the sensory nerve function of their feet. Diabetics who suffer from some degeneration of the retina should avoid exercises, such as weight lifting, that raise the pressure in the eye, increasing the risk of further damage to the retina.

Treatment of diabetes includes a diet, carefully controlled so that it provides just the right amount of carbohydrate for the body's needs. If adhered to, the diet can prevent some long-term complications of diabetes. Oral hypoglycaemic agents or administration of insulin may be needed to lower blood glucose levels.

(dī-əbē′tēz)
n

A deficiency condition involving carbohydrate metabolism and characterized by the habitual discharge of an excessive amount of urine.

Diabetes mellitus is a group of diseases characterized by elevated levels of glucose in the blood. Diabetes is caused by problems producing or responding to the hormone insulin. Insulin is produced in the pancreas by specialized cells called beta cells, in response to the presence of glucose absorbed through the gastrointestinal tract following a meal. Insulin promotes the uptake of glucose into muscle and fat cells, and it promotes the storage of excess glucose in the liver.

Excess blood glucose over time damages organs, particularly the eyes, kidneys, nerves, heart, and blood vessels. It is the leading cause of adult blindness, end-stage kidney disease, and lower limb amputations, and it is a major risk factor for heart attacks and strokes. Diabetes is classified into four major groups: type 1 diabetes (T1DM), type 2 diabetes (T2DM), other specific types, and gestational diabetes (GDM), occurring during pregnancy. Approximately 5 percent to 8 percent of the people of the industrialized world have diabetes, mostly (approximately 90 percent) type 2, which at least 16 million Americans have.

Type 1 Diabetes

Type 1 diabetes is caused by beta cell destruction, leading to insulin deficiency. T1DM was previously called insulin-dependent diabetes mellitus (IDDM), because patients who have it require insulin for survival. It was also called juvenile-onset diabetes mellitus, because most type 1 diabetics are children or young adults. At the time of diagnosis, about 85 percent to 90 percent of people with type 1 diabetes have antibodies directed against components of their beta cells, indicating that the immune system is responsible for the progressive and irreversible beta cell destruction.

Current evidence indicates a genetic component to T1DM. HLA (histocompatibility leukocyte antigen) genes are a group of genes on chromosome 6 that encode proteins that are part of the immune system. Normally the immune system defends the body against disease by destroying foreign cells, but in the case of type 1 diabetes, the body's immune system destroys its own beta cells.

Certain types of HLA genes are strongly associated with type 1 diabetes, and other types protect against its development. However, these HLA genes are neither necessary nor sufficient to cause or protect from type 1 diabetes. T1DM is therefore a "complex" genetic disorder, in which several genes interact with the environment to result in the disease. Scientists are currently working to identify these other genes, as well as environmental factors (e.g., toxins and viruses) that provoke the development of T1DM.

Type 2 Diabetes

Type 2 diabetes is itself a group of disorders caused by some combination of insulin resistance—which occurs when cells' ability to respond to insulin is compromised—and insulin deficiency, which occurs when the beta cells' ability to make insulin is compromised. T2DM has, in the past, been called adult-onset diabetes, because most people with T2DM were adults. It was also called non-insulin-dependent diabetes mellitus (NIDDM), because people with type 2 diabetes usually do not require insulin injections. In the Unites States, T2DM is especially prevalent among certain ethnic minorities, including African Americans, Mexican Americans, Asian Americans, and Native Americans.

Obesity is a potent risk factor for T2DM. In the last thirty years, due to increased caloric intake and physical inactivity, both of which contribute to obesity, there was an explosion in the prevalence of T2DM, and it started occurring at younger ages—even in children. In addition to its association with an unhealthy lifestyle, T2DM is known to have a strong genetic component.

Scientists have been searching throughout the genome for T2DM-susceptibility genes. One such gene, calpain 10 protease, was identified on chromosome 2. A common variant of this gene may predispose certain individuals to T2DM; however, the true significance of this gene variant remains to be determined. In addition, several candidate genes have shown some evidence of being involved in T2DM. However, the effect of any single candidate gene variant on the risk of developing T2DM is modest. A candidate gene is a gene for which prior knowledge of its function leads researchers to assess whether chemical variation in it is associated with a disease.

As of 2002 there was no clinically available genetic test to predict the onset of type 2 diabetes, but it is anticipated that with a better understanding of the roles of various genes in T2DM, it will eventually be possible to use multiple genetic tests to identify individuals at risk for T2DM and to predict which treatments will be most helpful in specific patients. Although genetic susceptibility plays an important role in determining the risk of developing T2DM, studies have shown that the disease can often be prevented through diet, physical activity, and weight loss.

Other Specific Types of Diabetes

The third category of diabetes, containing other specific types, includes nongenetic forms as well as single-gene forms of diabetes. One group of single-gene diabetes disorders are genetic defects in beta cell function. The most common of the genetic beta cell defects are the disorders known as MODY, or maturity onset diabetes of the young. MODY constitutes no more than 2 percent to 5 percent of all cases of diabetes. It often occurs in children and young adults and is characterized by decreased but not absent insulin production. It is inherited in an autosomal dominant manner, which means that an affected person has a 50 percent chance of passing on the disease-version of the gene with each pregnancy. Most, but not all, people receiving a MODY gene do develop diabetes.

There are at least six different genetic forms of MODY. MODY2 is caused by a mutation in a gene on chromosome 7 that makes a protein called glucokinase, which is an enzyme in beta cells that helps to provide a chemical signal needed for insulin release. The other MODYs involve mutations in genes that encode proteins called transcription factors, which allow beta cells to develop and function properly. These are hepatocyte nuclear factor 4-alpha (HNF4-alpha, causing MODY1, on chromosome 20), HNF1-alpha (causing MODY3, on chromosome 12), insulin promoter factor 1 (IPF1, causing MODY4, on chromosome 13), HNF1-beta (causing MODY5, on chromosome 17) and NeuroD1/beta2 (causing MODY6, on chromosome 2).

A very rare genetic insulin secretion disorder is maternally inherited diabetes and deafness (MIDD), caused by changes in the DNA of the mitochondria. The mitochondria are the energy powerhouses of the cell and the only part of the cell to contain DNA other than the nucleus, where most DNA is contained. MIDD and other mitochondrial disorders are maternally inherited because the fertilized egg has only mitochondria derived from the mother. The clinical features of MIDD can be similar to type 2 diabetes, and the hearing loss can be mild or even undetectable, except by special tests.

Another group of rare genetic diabetes types is characterized by extreme insulin resistance, which is defined as occurring when the ability of the body's cells to respond to insulin is severely compromised. Disorders of extreme insulin resistance include type A syndrome, leprechaunism, and Rabson-Mendenhall syndrome, and they are caused by inherited defects in the gene on chromosome 19 that makes the insulin receptor, a protein that allows cells to respond to insulin. Without properly functioning insulin receptors, insulin cannot work effectively. In addition to diabetes, individuals with insulin receptor defects may also have dental, genital, skin, and growth abnormalities. Most insulin receptor gene defects manifest in an autosomal recessive manner. That is, two defective copies of the gene are required for disease expression, and couples in which each partner has one defective copy (and in which neither is therefore affected) have a 25 percent chance of having an affected child, with each pregnancy.

Familial partial lipodystrophic diabetes (FPLD) is a rare condition in which children develop an unusual fat distribution at puberty, with little or no fat on their arms, legs, and trunk. They also develop insulin-resistant diabetes. FPLD is an autosomal dominant condition caused by mutations in the lamin A/C gene on chromosome 1. Another rare form of lipodystrophic diabetes is congenital (i.e., present at birth) generalized lipodystrophic (CGL) diabetes, which is autosomal recessive, and in about half of cases is due to mutations in the gamma-3-like gene (GNG3; also called the seipin gene), on chromosome 11.

Wolfram syndrome is a rare autosomal recessive condition presenting in childhood that includes diabetes mellitus as well as other problems, including deafness and deficiency of antidiuretic hormone. Mutations in the wolframin gene on chromosome 4 are responsible for some cases, but other cases appear to be caused by a gene in a different area of chromosome 4.

Another rare autosomal recessive childhood condition, thiamine-responsive megaloblastic anemia syndrome (TRMA), consists of several features, including blood abnormalities, deafness, and diabetes. TRMA, which responds to treatment with thiamine (a form of vitamin B), is a disorder caused by mutations in the thiamine transporter gene SLC19A2, on chromosome 1.

Transient neonatal diabetes (TNDM) is a condition in which infants are born requiring injected insulin but are able to make sufficient insulin later in infancy. Later in childhood or in adulthood, they may again develop diabetes, which may or may not require insulin treatment. Most cases of transient neonatal diabetes appear to be caused by the inheritance of an extra copy of a region of chromosome 6 from the father.

Many known genetic disorders other than those mentioned previously are associated with an increased risk of diabetes. Among those most strongly associated are Friedreich's ataxia, cystic fibrosis, and hemochromatosis.

Gestational Diabetes Mellitus

Hormones associated with pregnancy may cause diabetes in susceptible individuals. Although the diabetes goes away after the pregnancy, individuals who have had GDM are at increased risk of developing T2DM. Currently very little is known about the genetic basis of GDM. It is possible that some of the same genes responsible for T2DM are also involved in GDM.

Genetic Susceptibility to Complications

As mentioned above, diabetes is associated with complications involving the eyes, kidneys, blood vessels, and heart. However, not all individuals with diabetes develop these complications. There is increasing evidence that there are genes other than those that increase susceptibility to developing the disease that may influence susceptibility to developing its complications. These genes are not yet identified, but they are likely to interact with other known risk factors for complications, including poor blood-sugar control and increased blood-pressure and blood-cholesterol levels.

Bibliography

Internet Resources

American Diabetes Association. http://www.diabetes.org.

Joslin Diabetes Center. http://www.joslin.org.

Juvenile Diabetes Research Foundation International. http://www.jdrf.org.

National Institute of Diabetes and Digestive and Kidney Diseases. http://www.niddk.nih.gov.

Online Mendelian Inheritance in Man. Johns Hopkins University, and National Center for Biotechnology Information. http://www.ncbi.nlm.nih.gov/Omim.

—Toni I. Pollin and Alan R. Shuldiner

A general term referring to a variety of disorders characterized by polyuria and polydipsia. See diabetes mellitus and diabetes insipidus.

Dansk (Danish)
n. - sukkersyge

Nederlands (Dutch)
diabetes (suikerziekte)

Français (French)
n. - diabète

Deutsch (German)
n. - Diabetes, Zuckerkrankheit

Ελληνική (Greek)
n. - (παθολ.) (ζαχαρο)διαβήτης

Italiano (Italian)
diabete

Português (Portuguese)
n. - diabetes (m)

Русский (Russian)
диабет

Español (Spanish)
n. - diabetes

Svenska (Swedish)
n. - diabetes

中文（简体） (Chinese (Simplified))
糖尿病, 多尿症

中文（繁體） (Chinese (Traditional))
n. - 糖尿病, 多尿症

한국어 (Korean)
n. - 당뇨병

日本語 (Japanese)
n. - 糖尿病

العربيه (Arabic)
‏(الاسم) مرض السكري‏

עברית (Hebrew)
n. - ‮סוכרת, מחלת הסוכר‬

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